| Description | DZ2002, an orally active, reversible, and low-cytotoxic type III SAHH inhibitor (Ki=17.9 nM), exhibits significant immunosuppressive activity. It effectively prevents experimental dermal fibrosis by reversing the profibrotic phenotype in multiple cell types, making it useful for studying autoimmune diseases like lupus syndrome and systemic sclerosis. |
| In vitro | DZ2002 (0.1, 1, 10 µM; 96 h) inhibits the mixed lymphocyte reaction (MLR) response. DZ2002 (0.1, 1, 10 µM; 24 h) inhibits IL-12 and TNF-α production from both mouse peritoneal exudate cells and humanTHP-1 Cells. DZ2002 (0.1, 1, 10 µM; 64 h) inhibits expression of B7 (CD80/CD86) on differentiated THP-1 cells[1]. |
| In vivo | DZ2002 (2, 10, 50 mg/kg; i.p.; twice) blocks the DNFB-induced DTH response. (DNFB-induced DTH is a Th1 cell-mediated immune response, in which IL-12 is highly expressed and macrophages have been shown to play an important role). DZ2002 (0.08, 2 mg/kg; i.p.; single daily for 7 days) significantly suppresses a delayed-type hypersensitivity reaction as well as antibody secretion[1]. DZ2002 (50, 100 mg/kg; p.o.; single daily for 4 weeks) exerts a potent anti-fibrotic effect on dermal fibrosis by reducing the production of collagen, facilitating its degradation and regulating expression of various soluble factors in SSc mice model[2]. |
| molecular weight | 251.24 |
| Molecular formula | C10H13N5O3 |
| CAS | 33231-14-0 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility | DMSO: 45 mg/mL (179.11 mM), Sonication is recommended. |
| References | 1. Wu QL, et al. Inhibition of S-adenosyl-L-homocysteine hydrolase induces immunosuppression. J Pharmacol Exp Ther. 2005 May;313(2):705-11. 2. Zhang Z, et al. DZ2002 ameliorates fibrosis, inflammation, and vasculopathy in experimental systemic sclerosis models. Arthritis Res Ther. 2019 Dec 16;21(1):290. 3. He SJ, et al. Therapeutic effects of DZ2002, a reversible SAHH inhibitor, on lupus-prone NZB×NZW F1 mice via interference with TLR-mediated APC response. Acta Pharmacol Sin. 2014 Feb;35(2):219-29. |